Plasma Protein Systems, Cytokines, and Inflammation Outcomes Flashcards

1
Q

plasma protein systems

A

free floating proteins found in the blood, produced by the liver in a steady state during normal times, ramped up during inflammation; enzymatic cascades allow for amplification of immune response; all systems interact and also have regulatory components to turn it off

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2
Q

complement system

A
  • triggered by 3 different pathways
  • inflammation amplifier
  • attacks pathogens
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3
Q

3 pathways of complement system

A
  • classical pathway
  • alternative pathway
  • lectin pathway
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4
Q

classical pathway

A
  • initiated by antigen:antibody complex

- activates C1 complex to start cascade

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5
Q

lectin pathway

A
  • similar to classical pathway

- initiated by mannose-binding lectin (MBL)

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6
Q

alternative pathway

A
  • initiated by pathogen antigens

- binds free-floating C3b to create C3 Convertase

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7
Q

complement cascade products

A
  • C3a and C5a
  • C3b
  • C5b + C6-C9
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8
Q

C3a and C5a

A
  • anaphylotoxins (cause mast cell degranulation)

- chemotactic factors (leaves trail for leukocytes to follow to where they’re needed)

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9
Q

C3b

A

opsonins (tags pathogen for removal)

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10
Q

C5b + C6-C9

A

membrane attack complex (MAC)

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11
Q

C3b attaches to _____; ___ recognize opsonins

A

bacteria surfaces; phagocytes

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12
Q

membrane attack complex (MAC)

A

complement proteins insert themselves into the membrane of pathogens, creating pores; water and ions enter the cell; cell swells and lyses

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13
Q

complement system deficiencies: activation disorders

A

hard time turning it on; recurrent infections

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14
Q

complement system deficiencies: inhibitory disorders

A

hard time turning it off; ex: hereditary angioedema

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15
Q

coagulation system is activated by ____

A

endothelial damage and bleeding

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16
Q

coagulation system: intrinsic pathway is triggered by ___

A

vascular damage and platelets

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17
Q

coagulation system: extrinsic pathway is triggered by ___

A

external damage and tissue factor

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18
Q

coagulation system: intrinsic and extrinsic pathways share ____

A

final pathway

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19
Q

coagulation system forms a ____, which ____

A

fibrinous meshwork; prevents hemorrhage, traps pathogens, and prepares for repair

20
Q

coagulation system contributes to ____

A

inflammation (activates kinin and complement systems)

21
Q

kinin system is activated by ____

22
Q

kinin system is ____

A

pro-inflammatory

23
Q

product of kinin system is ____, which ____

A

bradykinin;
is similar to histamine; causes vasodilation, pain, smooth muscle contraction, increases vascular permeability, and leukocyte chemotaxis

24
Q

cytokines are soluble factors produced by ____

A

cellular mediators of inflammation and injured cells

25
there are many types of cytokines, the 3 main ones we focused on are ____
interleukins, interferon, and tumor necrosis factor-a
26
cytokines are pleiotropic, meaning ___
the effect depends on which cells are activated; development, maturation, localization, and activation of immune cells
27
cytokines have ____ targets
local and distant
28
interleukins
- macrophage and lymphocyte product - chemotactic - activates adaptive immune response (i.e., lymphocytes) - >30 types
29
IL-1
endogenous pyrogen, chemotaxis, leukocytosis, pro-inflammatory
30
IL-10
inhibits lymphocyte growth and macrophage activity, anti-inflammatory
31
interferon
- produced by virus-infected cells, macrophages, and lymphocytes - induces non-specific antiviral response and increases macrophage activity
32
tumor necrosis factor-a
- produced by macrophages and mast cells in response to PAMPs - increases endothelial adhesion molecules and macrophage activity
33
short term effects of tumor necrosis factor-a
induces fever (endogenous pyrogen) and increases PPS (plasma protein system) production
34
long term effects of tumor necrosis factor-a
promotes cachexia (wasting) and intravascular thrombosis (clotting throughout body)
35
termination of inflammation
- removal of an offending agent usually ends response | - checks exist to control course of inflammation
36
checks exist to control course of inflammation:
- neutrophil lifespan is short - inflammatory mediators degrade rapidly - anti-inflammatory cytokines are also produced
37
4 outcomes of acute inflammation
1) complete resolution 2) scarring 3) abscess formation 4) progression to chronic formation
38
complete resolution
structure and function recoverable
39
scarring
substantial damage to connective tissue
40
abscess formation
pus confined in a closed space; active proteases produce a fluid, increasing pressure; usually must drain
41
progression to chronic inflammation
body cannot remove offending agent; persistent bacteria/toxins or autoimmune diseases
42
chronic inflammation
- inflammation lasting 2 weeks or longer | - often related to an unsuccessful acute inflammatory response
43
causes of chronic inflammation
- high lipid wax content of microorganism (tuberculosis) - ability to survive inside the macrophage (chlamydia) - toxins and chemical irritants (alcohol abuse) - physical limitations (punctual plug) - particulate matter (asbestos, soot, etc.)
44
chronic inflammation has a dense infiltration of ____
lymphocytes and macrophages (also fibroblasts)
45
chronic inflammation has fibrosis, which is ____
thickening and scarring of connective tissue (collagen)
46
chronic inflammation has angiogenesis, which is ____
production of new blood vessels (VEGF)
47
chronic inflammation has granuloma formation, which is ____
walling off of the offending agent with collagen